Prior untargeted proteomic analysis in trabecular meshwork cells from POAG patients revealed the upregulation of the cochlin [126] and copine-1 [127] proteins, after comparison with age-matched control donors, suggesting that cochlin may disrupt the trabecular meshwork architecture and contribute to degradation of the extracellular matrix, resulting in cell aggregation, while copine-1 may play a role in the abnormal intracellular calcium signaling pathway in the glaucomatous trabecular meshwork. Here, CPNE1 is linked to open-angle glaucoma.